The most common causes of bacterial endophthalmitis are ocular surgery, usually cataract extraction, and endogenous spread from other infections such as meningitis, abdominal infection, endocarditis, and urinary tract infection.1 The clinical course is highly variable and depends on the virulence of the infecting organism, the quickness of diagnosis and administration of antibiotics, and the patient's underlying medical condition. According to the Endophthalmitis Vitrectomy Study2 conducted between 1990 and 1994, which studied the role of immediate vitrectomy and of intravenous antibiotics in the management of postoperative bacterial endophthalmitis, on post hoc data analysis, there was no difference in visual outcome whether or not an immediate vitrectomy was performed, except in a selected subgroup of patients. Furthermore, no ocular benefit was derived from the administration of systemic antibiotics. We reviewed the medical record of a patient who developed meningitis following a postoperative case of Streptococcus pneumoniae endophthalmitis. Since the advent of antibiotics, no other cases have been reported of systemic spread from a primary exogenous bacterial endophthalmitis, to our knowledge.

Report of a Case

An 81-year-old woman with Fuch corneal dystrophy complained of severe pain in her left eye 1 day following a penetrating keratoplasty and cataract extraction. The donor cornea was from a 3-year-old child who had drowned. On examination, she had hand motions/light perception only visual acuity, an intraocular pressure of 49 mm Hg, conjunctival chemosis, keratic precipitates on the corneal graft, a heavy cellular reaction in her anterior chamber, and a 4+ vitreous reaction that obscured retinal details in her left eye. The results of the remainder of her physical examination were normal. At this time, it was thought that she had postoperative endophthalmitis, and after consultation with physicians from both the retina and uveitis services, she was admitted for a vitreous tap and intravitreal injection as well as being started on a regimen of fortified topical antibiotics. She was treated with an intravitreal injection of vancomycin hydrochloride (1 mg), gentamicin sulfate (0.4 mg), and dexamethasone phosphate (0.4 mg), as well as topical vancomycin (50 mg/mL), tobramycin sulfate (14 mg/mL), and 1% prednisolone acetate. No systemic antibiotics were given. Ocular and orbital ultrasonography were performed and showed that no retinal detachment had occurred and no obvious extraocular inflammation was present. Cultures from the donor corneal rim and the vitreous humour both grew S pneumoniae sensitive to penicillin, clindamycin, and erythromycin.

On the seventh hospital day, the patient suddenly became confused and agitated and was found to have a stiff neck, a temperature of 38.9°C, and to be tachycardic. Her white blood cell count was 18.6 × 109/L. A lumbar puncture was performed that showed pink, turbid cerebrospinal fluid containing high levels of protein and abundant neutrophils and erythrocytes, as well as gram-positive diplococci. A diagnosis of meningitis secondary to endophthalmitis was made and a regimen of intravenous penicillin was started. Blood cultures obtained at that time later confirmed the presence of S pneumoniae sensitive to penicillin and chloramphenicol. Cerebrospinal fluid cultures yielded no bacterial growth. The patient recovered quickly once the intravenous antibiotics were given and was in her normal neurological state the next day.

During the patient's course in the hospital, the vision in her left eye did not improve and her intraocular pressure continued to rise despite maximal therapy. Magnetic resonance imaging of the head was performed and ruled out any further intraorbital or intracranial abscesses. A repeated orbital ultrasonogram showed dense vitreous opacities, vitreous membrane formation, and partial posterior vitreous detachment. After she was pronounced medically stable with her meningitis resolving uneventfully, a vitrectomy was performed, although her visual acuity never improved.

Comment

Most cases of bacterial endophthalmitis are caused by gram-positive organisms, notably Staphylococcus epidermidis, Staphylococcus aureus, and various Streptococcus species, including S pneumoniae.3,4 Endophthalmitis resulting from gram-negative organisms and fungi generally predisposes to an unfavorable clinical outcome. When compared with endophthalmitis due to other gram-positive organisms, infection by nonviridans Streptococcus species appears to result in the worst clinical outcome by a significant margin.4 This relatively poor outcome may be due to the greater degree of inflammatory response evoked by streptococcal exotoxins and enzymes.

In addition, there may be increasing reports of Streptococcus bacteremia and secondary endophthalmitis, particularly in patients with underlying medical conditions such as diabetes mellitus, malignant neoplasms, and human immunodeficiency virus infection.5 While the Endophthalmitis Vitrectomy Study2 clearly showed no ocular benefit from systemic antibiotics overall, there may have been specific causal subgroups that would derive benefit from intravenous antibiotics; however, data were insufficient for drawing statistical inferences. Furthermore, the study was designed to determine if there were any ocular, not systemic, benefits to using intravenous antibiotics.

Patients with bacterial endophthalmitis should be observed closely for signs or symptoms of metastatic spread. Although postoperative bacterial endophthalmitis is typically confined to the eye, this case report indicates that it is possible for the infection to spread to the central nervous system as well as other areas of the body. Aggressive treatment of endophthalmitis, possibly including intravenous antibiotics, may be considered in cases of particularly virulent pathogens and in patients with high-risk medical conditions.